Activation of Stat3 by v-Src is through a Ras-independent pathway

J Biomed Sci. 1998 Nov-Dec;5(6):446-50. doi: 10.1007/BF02255934.

Abstract

V-Src induces tyrosine phosphorylation of various cellular proteins and activates a number of signaling molecules including the Jak family of proteins tyrosine kinases and Stat (signal transducers and activators of transcription) proteins. Many cellular effects elicited by v-Src are mediated through Ras, a molecular switch linking growth factor receptors and non-receptor tyrosine kinases to many downstream effectors. In this report, we demonstrated that v-H-Ras and v-Src both induced cellular transformation. However, the activation of Jak1 and Stat3 were only observed in v-Src transformed cells. Using reporter gene assays, we further showed that activation of Stat3 and possibly of Jak1 by v-Src were mediated through a Ras-independent pathway. As Stat3 activation has recently been shown to be required for cellular transformation by v-Src, our results suggest that activation of the Jak-Stat pathway may serve as a modulator in some but not all transformation processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Line, Transformed
  • Cell Transformation, Neoplastic*
  • DNA-Binding Proteins / metabolism*
  • Genes, src*
  • Mice
  • STAT3 Transcription Factor
  • Signal Transduction*
  • Trans-Activators / metabolism*
  • Transfection
  • ras Proteins / metabolism*

Substances

  • DNA-Binding Proteins
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Trans-Activators
  • ras Proteins